For carcinogens such as polycyclic aromatic hydrocarbons, nitrosamines, and aromatic amines, it is thought that specific DNA adducts are more important than total DNA binding in the initiation of carcinogenesis. Thus for these carcinogens, it is more appropriate that the amount of these specific carcinogen-DNA adducts be the endpoint of the pharmacokinetic study rather than the total amount of DNA binding. The amount of DNA adduct formed could therefore be viewed as the "effective" dose for the induction of cancer. The "effective dose" can then be incorporated into low dose risk estimation procedures. We developed a general scheme for incorporating carcinogen-DNA adducts into low dose risk estimation procedures. With benzo(a)pyrene (BP) as a model carcinogen, dose-response curves for tumorigenesis and BP-DNA adducts are being simultaneously investigated in lung and forestomach of A/HeJ mice. The repair of BP-nucleoside adducts is also being studied. For species-to-species extrapolation of carcinogenic data, it is likely that both the qualitative and quantitative nature of the carcinogen-DNA adducts are important. The formation of BP-nucleoside adducts is being investigated in several species.